journal postinflammatory hyperpigmentation

5/19/2018 journal Postinflammatory Hyperpigmentation

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[ J u l y 2 0 1 0 V o l u m e 3 N u m b e r 7 ]202020202020202020202020202020202020

[ L I T E R A T U R E R E V I E W ]

ABSTRACTPostinflammatory hyperpigmentation is a common sequelae of inflammatory dermatoses that tends to affect darker

skinned patients with greater frequency and severity. Epidemiological studies show that dyschromias, including

postinflammatory hyperpigmentation, are among the most common reasons darker racial/ethnic groups seek the care of

a dermatologist. The treatment of postinflammatory hyperpigmentation should be started early to help hasten its

resolution and begins with management of the initial inflammatory condition. First-line therapy typically consists of

topical depigmenting agents in addition to photoprotection including a sunscreen. Topical tyrosinase inhibitors, such as

hydroquinone, azelaic acid, kojic acid, arbutin, and certain licorice extracts, can effectively lighten areas of

hypermelanosis. Other depigmenting agents include retinoids, mequinol, ascorbic acid, niacinamide, N-acetyl

glucosamine, and soy with a number of emerging therapies on the horizon. Topical therapy is typically effective for

epidermal postinflammatory hyperpigmentation; however, certain procedures, such as chemical peeling and laser

therapy, may help treat recalcitrant hyperpigmentation. It is also important to use caution with all of the above treatments

to prevent irritation and worsening of postinflammatory hyperpigmentation.

(J Clin Aesthetic Dermatol. 2010;3(7):2031.)

DISCLOSURE: Dr. Davis reports no relevant conflicts of interests. Dr. Callender is a consultant and speaker for Allergan, Coria, Medicis, Galderma,

Sanofi-Aventis, and Stiefel. She is also a researcher for Indendis, Medicis, and Merz.

ADDRESS CORRESPONDENCE TO: Valerie D. Callender, MD, Callender Skin & Laser Center, 12200 Annapolis Road, Suite 315, Glenn Dale, MD

20769; E-mail: [email protected]

Postinflammatory HyperpigmentationA Review of the Epidemiology, Clinical Features,

and Treatment Options in Skin of Color

aERICA C. DAVIS, MD; a,bVALERIE D. CALLENDER, MDaCallender Skin & Laser Center, Glenn Dale, Maryland;

a,bDepartment of Dermatology, Howard University College of Medicine, Washington, DC

Postinflammatory hyperpigmentation (PIH) is an

acquired hypermelanosis occurring after cutaneous

inflammation or injury that can arise in all skin types,

but more frequently affects skin-of-color patients, including

African Americans, Hispanics/Latinos, Asians, Native

Americans, Pacific Islanders, and those of Middle Eastern

descent. PIH can have a significant psychosocial impact on

skin-of-color patients (Fitzpatrick skin types IV through

VI), as these pigmentary changes can occur with greater

frequency and severity in these populations1 and oftentimesbe more obvious in darker skin. However, there is a wide

variety of safe and effective treatments for PIH in skin of

color, including topical depigmenting agents, chemical

peels, and laser and light therapy. Therefore, this article

reviews the etiology, pathogenesis, clinical manifestations,

and treatment options for PIH in skin of color.

EPIDEMIOLOGY

Table 1 shows the worldwide prevalence of pigmentary

disorders, excluding vitiligo, in various ethnic

populations. These figures typically include

postinflammatory hyper- or hypopigmentation although

melasma and solar lentigines may also be included.

Multiple epidemiological studies have shown that PIH

tends to occur more commonly among skin-of-color

patients compared to Caucasian patients.2,3 In 1983,

Halder et al2 published a study comparing the mostcommon dermatoses seen in African American and

Caucasian patients. Pigmentary disorders, other than

vitiligo, were the third most common dermatoses among

African-American patients (9%), but were the seventh

most common among Caucasian patients (1.7%). A more

recent study in 20073 confirmed these findings showing


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dyschromias to be the second most common diagnosis

among African-American patients, but dyschromias failed

to make it into the top 10 most common diagnoses for

Caucasian patients. Of interest, in a study conducted in

Singapore,4 the authors note that PIH tended to also be

more prevalent among Asians with darker skin, such as

Malays and Indians, than those with lighter skin, such as

the Chinese, suggesting that the degree of pigmentation

rather than race/ethnicity may be more contributory to

the development of PIH.

ETIOLOGYMany types of inflammatory dermatoses or cutaneous

injuries can cause pigmentary changes; however, there are

some diseases that show a proclivity to develop PIH rather

than hypopigmentation. A wide range of etiologies for PIH

exists including infections such as dermatophytoses or

viral exanthems, allergic reactions such as those from

insect bites or a contact dermatitis, papulosquamous

diseases like psoriasis or lichen planus, medication-induced

PIH from hypersensitivity reactions, or cutaneous injury

TABLE 1. Worldwide prevalence of pigmentary disorders (excluding vitiligo) in skin of color

AUTHOR YEAR STUDY POPULATION PREVALENCE RANK LOCATION

Halder

2

19801983

2,550: 78.4% African Americans,

21.6% Caucasian 9% black; 1.7% white

3/13 black,

7/10 white Washington, DC

Chua-Ty4 1989199074,589: 77.2% Chinese, 9.9% Indian,7.6% Malay, 5.3% Other

1.8% Chinese, 2.7% Malay,2.3% Indian, 1.2% other

10/10 Singapore

Nanda116 1992199610,000: 88% Kuwaitis, 8% other Arabs,4% non-Arabs; all children

0.42% 33/74 Kuwait

Child117 1996461: black (African, Afro-Caribbean,mixed race); 187 children, 274 adults

1.6% children, 3.4% adults8/14 children,7/29 adults

London, England

Hartshorne118 19997,029: 76.1% black, 10.9% Caucasian,6.7% Indian, 6.1% colored (mixed race)

0.7% black, 0.1%Caucasian, 0.3% Indian,0.5% colored (mixed race)

22/91 overall Johannesburg, South Africa

Dunwell119 20011,000: 95.6% Afro-Caribbean, 0.8%Caucasian, 2.2% Indian, 1.4% Chinese

22.8%* (includes PIH,melasma, solar lentigines)

3/18 Kingston, Jamaica

Sanchez120Published2003

3,000: Latino (1,000 private practice,2,000 hospital-based clinic)

6% private practice,7.5% hospital-based clinic

7/12 private,6/12 hospital

New York, New York

Arsouze121 2004 1,064: black (African, Afro-Caribbean;FST V and VI); 228 children, 836 adults

6.1% children, 9.2% adults 6/16 children,2/20 adults

Paris, France

Alexis3 20042005 1,074: black and white19.9% of diagnoses in

blacks#, not in whites2/14 New York, New York

El-Essawi122Published2007

401: Arab Americans (33.7% Lebanesedescent)

56.4% uneven skin tone,55.9% skin discoloration

Top 2 skinconcerns outof 10

Detroit, Michigan

*Data not separated by race/ethnicity#Subsequent visits by the same patient were included in the data pool

PIH = Postinflammatory hyperpigmentationFST = Fitzpatrick skin types


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from irritants, burns, or cosmetic procedures (Figure 1).5

However, very common causes of PIH in skin of color

include acne vulgaris, atopic dermatitis, and impetigo. In

fact, PIH is a particularly common sequela after acne in

dark-skinned patients (Figure 2). A study in 2002

evaluating acne in skin of color found that 65.3 percent of

African-American (N=239), 52.7 percent of Hispanic

(N=55), and 47.4 percent of Asian (N=19) patients

developed acne-induced PIH.6 Pseudofolliculitis barbae

(PFB) is another common inflammatory dermatosis,

particularly among African Americans, that results in PIH

and is estimated to have a prevalence rate between 45 and

83 percent.7,8 In a study by Perry et al9 of 71 African

American and Hispanic patients with PFB, 90.1 percent of

patients reported hyperpigmentation; therefore, the

authors suggest that PIH may be a major clinical finding in

PFB (Figure 3).

PATHOGENESISPIH results from the overproduction of melanin or an

irregular dispersion of pigment after cutaneous

inflammation.10 When PIH is confined to the epidermis,

there is an increase in the production and transfer of

melanin to surrounding keratinocytes. Although the exact

mechanism is unknown, this rise in melanocyte activity

has been shown to be stimulated by prostanoids,cytokines, chemokines, and other inflammatory

mediators as well as reactive oxygen species that are

released during the inflammatory process. Multiple

studies have demonstrated the melanocyte-stimulating

properties of leukotrienes (LT), such as LT-C4 and LT-D4,

prostaglandins E2 and D2, thromboxane-2, interleukin

(IL)-1, IL-6, tumor necrosis factor (TNF)-, epidermal

growth factor, and reactive oxygen species such as nitric

oxide.1,5,11,12

PIH within the dermis results from inflammation-

induced damage to basal keratinocytes, which release large

amounts of melanin. The free pigment is then phagocytosed

by macrophages, now called melanophages, in the upper

dermis and produces a blue-gray appearance to the skin at

the site of injury.13,14

CLINICAL MANIFESTATIONSPIH typically manifests as macules or patches in the

same distribution as the initial inflammatory process. The

location of the excess pigment within the layers of the skin

will determine its coloration. Epidermal hypermelanosis

will appear tan, brown, or dark brown and may take

months to years to resolve without treatment. 1

Hyperpigmentation within the dermis has a blue-gray

appearance and may either be permanent or resolve over

a protracted period of time if left untreated.1,15 The

intensity of PIH may also correlate with higher skin

phototypes (Figures 4A and 4B), although studies are

needed to confirm this finding. In addition, PIH can

worsen with ultraviolet (UV) irradiation or with persistent

or recurrent inflammation.16

TREATMENTThe management of PIH should begin first with

addressing the underlying inflammatory dermatosis.

Initiating treatment early for PIH may help hasten its

resolution and prevent further darkening. However, it is

important to always be mindful of the potential thetreatment itself has to cause or exacerbate PIH by causing

irritation.17 There are a variety of medications and

procedures in addition to photoprotection that can safely

and effectively treat PIH in darker skinned patients.

Topical depigmenting agents, such as hydroquinone,

azelaic acid, kojic acid, licorice extract, and retinoids, can

be effective alone or in combination with other agents, and

procedures such as chemexfoliation and laser therapy can

also be incorporated into the management strategy if

needed (Table 2). Of note, topical agents are typically used

to treat epidermal PIH as deeper pigmentation does not

respond well to these agents.16

Figure 1. Postinflammatory hyperpigmentation after

light electrodessication for dermatosis papulosa nigra

Figure 2. Acne-induced PIH in a

patient with Fitzpatrick skin type V

Figure 3. African-American female

with hirsutism and pseudofolliculitis

barbae with PIH


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Photoprotection. An integral part in the treatment of

PIH that should not be overlooked or underestimated is the

importance of photoprotection to prevent the worsening of

PIH. Patients should be educated on the use of daily broad-

spectrum sunscreen with a sun protection factor (SPF) of

30 and sun-protective measures, such as avoidance and

protective clothing. This is particularly true for those with

higher skin phototypes who may not normally wear

sunscreen, but also may not realize the darkening effects

UV irradiation has on hyperpigmentation. In fact, a study

analyzing data from the 1992 National Health Interview

Survey of 1,583 African Americans regarding sun-

protection behaviors found that only a minority of the

respondents were very likely to use sunscreen (9 vs. 81%

who were unlikely to use it), wear protective clothing

(28%), or stay in the shade (45%).18

Although clinical studies have shown that serum vitamin

D levels are reduced in sunscreen users compared to

nonusers, these levels are still within normal range.19,20 This

is particularly important for dark-skinned individuals who

may already be at risk for vitamin D deficiency due to

inherently higher melanin concentrations in the skin.21 The

American Academy of Dermatology has released a position

statement on vitamin D, which states that groups at risk for

vitamin D deficiency, including dark-skinned individuals,

may need a daily total dose of 1000IU of vitamin D, through

diet and supplementation, according to the current United

States Department of Agriculture Dietary Guidelines.22

Therefore, proper counseling and education involvesencouraging the daily use of a broad-spectrum sunscreen

with an SPF of 30; sun-protective measures, such as

avoidance and protective clothing; the intake of foods rich

in vitamin D, such as salmon, fish liver oils, and fortified

foods; and vitamin D supplementation.

Medical therapy.Hydroquinone (HQ). The mainstay

of treatment for PIH remains HQ. It is a phenolic compound

that blocks the conversion of dihydroxyphenylalanine

(DOPA) to melanin by inhibiting tyrosinase.10,23 Its

mechanism of action may also involve inhibition of

deoxyribonucleic acid (DNA) and ribonucleic acid (RNA)

synthesis, selective cytotoxicity toward melanocytes, and

melanosome degradation.24,25 HQ is commonly used at

concentrations from 2 to 4% but can be prescribed in

strengths up to 10% and is available over the counter (OTC)

at 2% in the United States.

Hydroquinone monotherapy can be effective in treating

PIH, but more recently HQ has been formulated with other

agents, such as retinoids, antioxidants, glycolic acid,

sunscreens, and corticosteroids, to increase efficacy.10

Cook-Bolden et al26 conducted a 12-week, open-label study

of microencapsulated HQ 4% and retinol 0.15% with

antioxidants in the treatment of 21 patients (81%

Fitzpatrick skin types IVVI) with PIH (n=17) and

melasma (n=4). There were significant decreases in lesion

size, pigmentation, and disease severity from Week 4 to the

study endpoint (all P


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hypopigmentation of the surrounding normal skin that has

been treated with HQ (halo effect).23 Patients may also

develop exogenous ochronosis (EO) (Figure 5) where

homogentisic acid accumulates within the dermis causing

hyperpigmentation and papules on sun-exposed areas

where HQ has been applied to the skin.10,34,35 EO is typically

associated with frequent use of very high concentrations of

HQ on a long-term basis although EO can still occur with

short-term use of 1 to 2% HQ.36,37 It is most commonly

reported in blacks in South Africa, where the prevalence of

EO is high.6 In the United States, a low number of

hydroquinone-induced EO cases have been reported.38

However, there has been a recent rise in the illicit use of

high-concentration HQ available OTC in ethnic stores in

the United States.38

In 2006, the United States Food and Drug Administration

(FDA) released a statement proposing a ban on all OTC HQ

agents based on rodent studies, which suggested that oral

HQ may be a carcinogen.37 However, there have been no

reports of skin cancers or internal malignancies associatedwith topical HQ use.23 To date, a final ruling by the FDA is

still pending.

Mequinol.A derivative and alternative to hydroquinone

is 4-hydroxyanisole or mequinol. Although the two agents

are related, mequinol is thought to be less irritating to the

skin than HQ.39 The drug is available by prescription in a 2%

concentration and is typically formulated with 0.01%

tretinoin, a retinoic acid and penetration enhancer.40 The

mechanism by which mequinol causes depigmentation may

involve a competitive inhibition of tyrosinase; however, the

exact pathway is unknown.40 Several large clinical studies

have shown that mequinol effectively treats solar lentigines

in all patients39,41 including ethnic populations42; however,

only small clinical studies exist that evaluate its

effectiveness in the treatment of PIH.4345 One such study43

compared mequinol 2%/tretinoin 0.01% to HQ 4% cream in

61 skin-of-color patients with mild-to-moderate facial PIH.

Patients applied each medication to contralateral sides of

the face for 12 weeks. Topical mequinol/tretinoin was

shown to be noninferior to 4% HQ as 81 and 85 percent of

patients experienced clinical success on the mequinol-

treated and the HQ-treated sides of the face, respectively.

Retinoids. Retinoids are structural and functional

analogues of vitamin A, and are effective alone or in

combination with other agents for the treatment of PIH in

ethnic patients. Retinoids exert multiple biological effects

that result in skin lightening including the modulation of cell

proliferation, differentiation, and cohesiveness; induction of

apoptosis; and expression of anti-inflammatory properties.46

Topical tretinoin, all-trans-retinoic acid, is a naturally

occurring metabolite of retinol and first-generation

retinoid.46 Concentrations range from 0.01 to 0.1% and

tretinoin can be formulated in creams, gels, and microsphere

gels, which allows for the controlled release of tretinoin

leading to less irritation.47,48A 40-week, randomized, double-

blind, vehicle-controlled clinical trial was conducted with 54

black patients to determine the safety and efficacy of 0.1%tretinoin in the treatment of PIH. Tretinoin was significantly

more effective than vehicle in lightening PIH lesions when

assessed by clinical (P


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gels in 0.1 to 0.3% concentrations; whereas, formulations of

tazarotene include 0.05 and 0.1% creams or gels. Both

agents have been shown in clinical studies to safely and

effectively treat PIH, particularly acne-induced PIH, in

darker skinned individuals.49,50 Isotretinoin (13-cis-retinoic

acid) is a naturally occurring, first-generation retinoid that

is available in both oral and topical formulations. Oral

isotretinoin is very effective in the treatment of severe

acne; however, there has also been a case reported in theliterature of significant resolution of PIH after oral

isotretinoin therapy in an Asian patient.51

Azelaic acid. Naturally occurring as a dicarboxylic acid

isolate from the organism responsible for Pityriasis

versicolor, azelaic acid (AA) has been shown to be effective

in the treatment of PIH.10 AA has several mechanisms by

which it depigments the skin including tyrosinase inhibition

as well as selective cytotoxic and antiproliferative effects

toward abnormal melanocytes through the inhibition of

DNA synthesis and mitochondrial enzymes.52,53 Available

formulations include a 15% gel, typically used in the

treatment of rosacea, or a 20% cream that is commonly

used for acne vulgaris and melasma in addition to PIH. Lowe

et al54 conducted a randomized, double-blind, vehicle-

controlled trial of 52 patients (Fitzpatrick skin types IVVI)

with facial hyperpigmentation including PIH and melasma

to determine the safety and efficacy of 20% AA cream.

Patients treated with AA showed greater decreases in

pigmentary intensity after 24 weeks of treatment versus

vehicle as measured by the investigators subjective scale

(P=0.021) and chromometric analysis (P


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of depigmentation at work.69 Multiple double-blind,

controlled clinical trials have shown the safety and efficacy

of NAG alone or NAG/niacinamide combination therapy to

significantly lighten hyperpigmentation secondary to solar

radiation in Caucasian and Japanese patients.68,69 NAG was

generally well tolerated with mild-to-moderate skin

irritation reported in a small number of patients. However,

large clinical studies are still needed to determine the role

of NAG in the management of PIH in all skin types.Ascorbic acid. L-ascorbic acid (AA) or vitamin C is a

naturally occurring antioxidant obtained from certain fruits

and vegetables.23AA causes skin lightening by interacting

with copper ions at the tyrosinase active site and by

reducing oxidized dopaquinone, a substrate in the melanin

synthetic pathway.23,70 In addition to skin lightening, other

advantages of AA include not only antioxidant effects but

some studies also demonstrate anti-inflammatory and

photoprotective properties.7176 However, early

formulations of AA were unstable so esterified derivatives,

such as ascorbyl-6-palmitate and magnesium ascorbyl

phosphate, were created.71AA is typically used in 5 to 10%

concentrations and can be formulated with other

depigmenting agents, such as hydroquinone, which is

generally well tolerated in skin of color given the good

safety profile of AA.10,40AA and its derivatives have been

shown to be safe with some efficacy in certain racial/ethnic

populations including Latino and Asian patients; however,

most studies involved the treatment of melasma and did

not include PIH.77,78

Licorice. Licorice root extract (Glycyrrhiza glabra,

Glycyrrhiza uralensis) is a common ingredient found in

many skin-lightening cosmeceuticals,40 and is also used in

the treatment of a wide variety of diseases even outside the

scope of dermatology due to its anti-inflammatory,

antiviral, antimicrobial, and anticarcinogenic properties.79

Some of the active ingredients in licorice root extract

include glabridin, which inhibits tyrosinase and possesses

anti-inflammatory effects,80,81 and liquiritin, which does not

inhibit tyrosinase but causes depigmentation by melanin

dispersion and removal.82 There are very few clinical trials

that study the utility of licorice root extracts in the

treatment of dermatological conditions. One study

conducted in 20 Egyptian women showed that topical

liquiritin cream (1g/day) for four weeks was both safe and

effective in the treatment of melasma.82 Side effects were

minimal. Further clinical studies with racial/ethnic patientsare needed to evaluate the efficacy of licorice root extract

in the treatment of PIH.

Soy. The activation of protease-activated receptor 2

(PAR-2) cell receptors found on keratinocytes mediates

the transfer of melanosomes from melanocytes to

surrounding keratinocytes.83 Soy proteins, such as soybean

trypsin inhibitor (STI) and Bowman-Birk inhibitor (BBI),

inhibit the activation of these cell receptors, and as a result,

phagocytosis of melanosomes into keratinocytes is reduced

leading to reversible depigmentation.83 Soy is now being

formulated alone or in combination with other agents

including retinol and sunscreen into cosmeceuticals,

particularly moisturizers, to help reduce the signs of

photodamage as well as PIH in all skin types.8486A 16-week,

double-blind, placebo-controlled, clinical study of African-

American, Hispanic, and Asian patients with Fitzpatrick

skin types III to V and acne-induced PIH was conducted to

determine the safety and efficacy of an OTC anti-acne

treatment containing salicylic acid, retinol, and total soy.87

There was a significant improvement in PIH with the soy

formulation from baseline to study endpoint as well aswhen compared to placebo. Soy-containing products are

generally well tolerated.40 However, more large-scale

clinical trials in skin of color are still needed.

Surgical therapy. Chemical peels. In 2008, chemical

peeling was the fourth most common nonsurgical cosmetic

procedure performed in the United States,88 and

dyschromias, such as PIH, are one of the most common

indications for this procedure in skin of color.89 For darker

skinned individuals, superficial chemical peels, which

penetrate into the papillary dermis,90 are generally well

tolerated with good clinical results.10 However, care should

be taken in selecting and using the specific chemical peel

to avoid irritation, which can worsen PIH and lead to other

complications, such as new areas of dyspigmentation,

keloid formation, and hypertrophic scarring.91 A detailed

history, including other dermatological conditions, current

oral and topical medications, history of herpes simplex

virus (HSV) infection, past reactions to other cosmetic

procedures, and a skin examination should be obtained

prior to the procedure.89,90,92

Glycolic acid (GA), found in sugarcane, is a naturally

occurring alpha-hydroxy acid (AHA) that induces

epidermolysis, disperses basal layer melanin, and increases

dermal collagen synthesis.90,93 GA concentrations range

from 20 to 70%, and neutralization with water or sodium

bicarbonate is required to terminate the peel. Burns et al94

conducted a 22-week clinical study of 16 African-American

patients with Fitzpatrick skin types IV to VI and facial PIH.

Patients were randomized to either the control group

receiving 2% hydroquinone/10% GA gel and 0.05%

tretinoin or the peel group receiving the same topical

regimen plus six GA peels (5068%) at three-week

intervals. Significant clinical improvement from baseline

was noted in the peel group by subjective measures

(p


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improvements were also noted in greasiness, dryness, and

scaliness by clinical exam. The safety and efficacy of SA

peels in the treatment of PIH has also been demonstrated

in even higher skin phototypes V and VI.96

Superficial chemical peels can also be obtained using

trichloroacetic acid (TCA) or Jessners solution, and both

agents have been efficacious in the treatment of

melasma.97,98 However, clinical evidence supportive of the

use of these agents for PIH in skin of color is lacking.Most superficial chemical peeling agents are well tolerated

by Fitzpatrick skin types IV to VI. Common side effects

include erythema, burning sensation, PIH, reactivation of

HSV, superficial desquamation, and vesiculation.89 Other

complications include hypopigmentation, hypertrophic

scarring, and keloid formation. Patients should also be

educated on the importance of photoprotection to prevent or

avoid worsening PIH after chemical peeling.

Laser and light-based therapies. Although topical

skin-lightening agents remain the treatment of choice for

PIH, lasers and light sources may be an effective adjunct to

therapy or alternative for treatment failures. However,

there is a paucity of literature specifically evaluating the

use of devices in the treatment of PIH in all skin types.

Green (510nm, 532nm), red (694nm), or near-infrared

(755nm, 1064nm) lasers are pigment-specific and generate

light used to selectively target intracellular melanosomes.99

However, due to the wide absorption spectrum of melanin

(250nm1200nm), laser energy intended for deeper

targets can be absorbed within the pigmented epidermis,

which can lead to complications such as dyschromias,

blistering, and scars.100

Typically, energy from short wavelength lasers is more

efficiently absorbed by epidermal melanin while longer

wavelengths penetrate deeper with more selective

absorption by dermal targets making them safer to use for

darker-skinned patients.100 The use of longer pulse

durations and cooling devices can also provide a greater

margin of safety while still maintaining efficacy in darker

skinned individuals.100 There have been case reports of the

successful treatment of PIH with blue light photodynamic

therapy, neodymium-doped yttrium aluminum garnet

(Nd:YAG) laser, and fractional photothermolysis in darker

skin types101103; however, larger clinical studies are needed

to evaluate the role of these lasers as well as other devices,

such as intense pulsed light, in the treatment of PIH.

Cosmetic camouflage. Cosmetic camouflage may beuseful to conceal pigmentary disorders, vascular lesions,

scars, and chronic skin conditions that are not amenable to

medical or surgical treatments.104 These coverage techniques

can help alleviate the patients distress regarding their

appearance and significantly improve quality of life.105,106

Camouflage can be particularly useful in darker skinned

individuals where pigmentary changes may be more

noticeable and when highly visible parts of the body are

affected by the disease, such as the face, neck, and hands.107

The characteristics of a good cosmetic cover include a

natural appearance and non-greasy feel, and the cover should

also be waterproof, long lasting, and noncomedogenic with

easy application.108 There are four basic foundations: oil-

based for dry skin, water-based for dry-to-normal skin, oil-

free for oily skin, and water-free, which mixes oils with waxes

to form thicker creams that can incorporate higher amounts

of pigment to match the patients normal skin color.104

Cosmetic covers can be applied for subtle coverage up to full

concealment,109 and color correctors use the lesions color

opposite to neutralize its intensity.104

Emerging therapies. Continued research is constantlyfueled by the demand for newer, more effective

depigmenting agents. Undecylenoyl phenylalanine 2% has

been shown to safely and effectively treat solar lentigines

in a recent randomized, double-blind, vehicle-controlled

clinical trial.110 There have also been case reports and

clinical studies that have shown that topical 5%

methimazole,111 aloesin,112 and dioic acid113 can successfully

treat hyperpigmentation secondary to a variety of

etiologies. Other agents that have shown some

depigmenting properties but require further research

include 4-(1-phenylethyl)1,3-benzenediol, paper mulberry,

ellagic acid, quinolines, piperlonguminine, luteolin,

calycosin, emblica, and multivitamins.10,114,115

CONCLUSIONIn skin of color, postinflammatory hyperpigmentation

can be a common yet troubling sequelae of cutaneous

inflammation. However, there are many safe and effective

treatments for this patient population including a variety of

topical depigmenting agents. It is important to initiate

treatment early while at the same time use caution with

these agents to prevent further worsening of the

hyperpigmentation. Procedures such as chemical peeling

and laser therapy provide alternatives or adjuncts to

topical therapy. Adding sunscreen to the treatment

regimen and patient education regarding sun protection

measures will also be beneficial in the management of

patients with PIH.

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